Abstract
BackgroundOur aim was to investigate dynamic changes in hepatitis B virus (HBV) surface antibody (HBsAb) titer and the associated risk of HBV reactivation and clinical course in patients with HBV surface antigen negative/core antibody positive (HBsAg−/HBcAb+) serostatus during antirheumatic therapy with biologic agents.MethodsIn a prospective study from January 2013 to June 2017, we monitored the HBV serostatus of HBsAg−/HBcAb+ patients undergoing biologic therapy for rheumatic diseases. From HBsAb titers at baseline and subsequent time points, we calculated the person-years (PY) contributed by patients with different HBsAb levels: < 10 mIU/mL (negative); 10–100 mIU/mL (low); and > 100 mIU/mL (high). We analyzed the incidence of detectable HBV DNA and HBV reactivation in each group, and documented the clinical courses of patients.ResultsAmong 380 participants, 83 (21.8%) had baseline HBsAb < 10 mIU/mL, 156 (41.1%) HBsAb 10–100 mIU/mL, and 141 (37.1%) HBsAb > 100 mIU/mL. Total PY at study end were 169.3 PY from the HBsAb-negative group, 362.7 PY from the low-titer group, and 285.8 PY from the high-titer group. Seventeen patients had detectable HBV DNA, with respective incidence rates in negative, low- and high-titer groups of 4.7/100 PY, 2.5/100 PY, and 0/100 PY. Two HBsAb-negative patients subsequently developed HBV reactivation, an incidence of 1.2/100 PY.ConclusionsThe risk of HBV reactivation varied with HBsAb titer, which changed during biologic therapy. Neither HBV DNA nor reactivation were detected in patients with HBsAb > 100 mIU/mL, whereas HBV DNA without reactivation occurred periodically in patients with HBsAb 10–100 mIU/mL; HBsAb-negative serostatus was associated with a risk of HBV reactivation.
Highlights
Our aim was to investigate dynamic changes in hepatitis B virus (HBV) surface antibody (HBsAb) titer and the associated risk of HBV reactivation and clinical course in patients with HBV surface antigen negative/core antibody positive (HBsAg−/Hepatitis B virus core antibody (HBcAb)+) serostatus during antirheumatic therapy with biologic agents
HBV surface antibody (HBsAb) titer changes, HBV DNA, and HBV reactivation during follow-up Figure 1 tracks the changes of HBsAb titer and PYs contributed to the ‘negative’, ‘low’, and ‘high’ groups throughout the study
The HBsAb titer varied during follow-up; most participants remained in the same titer group as at baseline, and a proportion exhibited a declining trend in HBsAb titer, while the titer rose in a few
Summary
Our aim was to investigate dynamic changes in hepatitis B virus (HBV) surface antibody (HBsAb) titer and the associated risk of HBV reactivation and clinical course in patients with HBV surface antigen negative/core antibody positive (HBsAg−/HBcAb+) serostatus during antirheumatic therapy with biologic agents. Hepatitis B virus (HBV) reactivation has emerged as a major complication in patients with hepatitis B surface antigen-negative/core antibody-positive serostatus (HBsAg− /HBcAb+; which indicates a past HBV infection since resolved) who receive biologic agents to treat rheumatic diseases such as rheumatoid arthritis, ankylosing spondylitis, and psoriasis/psoriatic arthritis [1,2,3,4,5,6]. Patients with high baseline HBsAb titer (> 100 mIU/mL) preceding chemotherapy or immunosuppressive therapy had lower risk of HBV reactivation [10, 11]. There has been no study exploring if the risk of HBV reactivation varies followed by the change of HBsAb titer during biologic therapy
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